In contrast to normocomplementemic rabbits, C6-deficient rabbits fail to develop respiratory distress and sudden death upon intravenous injection of arachidonic acid. Experiments will be done to restore the response to arachidonic acid of homozygous C6-deficient rabbits by exchange transfusion with large volumes of normocomplementemic whole blood. In addition to C6 defiency, other mechanisms will be explored that may explain the failure of C6-deficienct animals to respond to the injection of arachidonic acid. These include the capacity of lung tissues from C6-deficient rabbits to generate prostaglandin endoperoxides and thromboxanes, and the response of the lung vessels of C6-deficient rabbits to arachidonic acid and thromboxanes. Investigations will be performed on the reaction mechanisms of tissue factor (thromboplastin) with the complement system. Efforts will be directed to identify the complement components that react with tissue factor and to describe the mechanism of these reactions. BIBLIOGRAPHIC REFERENCES: Chow, Y.M., Giavedoni, E.B. and Dalmasso, A.P.: Properties of the lesion induced by complement on erythrocyte membranes. Fed. Proc., 1977, 36:1282. Mason, R.P., Giavedoni, E.B. and Dalmasso, A.P.: Complement induced decrease in membrane mobility: introducing a more sensitive index of spin label motion. Biochemistry, 1977, in press.